Potassium is the most abundant cation in the body (35-40 mmol/kg in haemodialysis patients [1]), although only 2% of the pool is located extracellularly [2]. Whereas, on a short-term basis, serum potassium is regulated by the shift of potassium between the intracellular and the extracellular compartment by insulin, cathecolamines, acid-base balance, and osmolarity; kidneys are responsible for long-term potassium homeostasis [2]. Patients with end-stage renal disease are at high risk of hyperkalaemia [3-6], which may present itself as generalised weakness, paralysis, and cardiac arrhythmia [2]. Recovering potassium homeostasis is thus an important objective of dialysis. Still, considering that its location is mainly intracellular, which connects to the pharmacological concept of great distribution volume, its removal during a haemodialysis session is quantitatively modest (between 40 and 80 mmol corresponding to 1-2% of total body potassium) [1]. As a consequence, even if, in order to be suitable, potassium removal during dialysis should be equal to the amount accumulated during the inter-dialytic phase, in clinical practice the potassium concentration in the dialysate is usually adjusted with the suboptimal goal of avoiding pre-dialysis hyperkalaemia [7].